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Biomedical subjects

G Perez

Publications and source records attributed to G Perez.

At least 127 records · Page 7Linked to original sources
PubMed1976

[The participation of the cholinergic system in the genesis of the reflex vasodilatation in the gracilis muscle of the dog (author's transl)].

These experiments were undertaken to demonstrate the participation of the cholinergic system in the reflex vasodilatation in the gracilis muscle of the dog evoked by rapid i.v. injection of norepinephrine. The analysis of the integrated areas of vasodilatation curves after pretreatment with atropine showed a significant decrease of the reflex vasodilatation suggesting the participation of the cholinergic system to the mechanism underlying the phenomenon. The residue vasodilatation was completely abolished by the subsequent i.a. administration of phentolamine. On the other hand, guanethidine too could, also without pretreatment with atropine, nullify the reflex vasodilatation. This effect, therefore, does not permit the ruling out of the existence of a cholinergic component in the reflex vasodilatation since the actions of these drugs are not yet completely known.

Animals↗
PubMed1976

Cation-exchange chromatography of guanidine derivatives in plasma of patients with chronic renal failure.

Guanidine derivatives are suspected of contributing to the toxic manifestations of uremia. We describe a method for measurement of guanidine derivatives in 5-ml samples of plasma by liquid chromatography. Concentrations of guanidinosuccinate and guanidinobutyrate in plasma were significantly increased both in undialyzed patients with chronic renal failure (5.54 +/- 0.94 and 17.5 +/- 4.07 mg/liter) and those undergoing maintenance hemodialysis (2.35 +/- 0.41 and 19.4 +/- 3.99 mg/liter) when compared to healthy controls (less than 0.4 and 1.0 +/- 0.3 mg/liter, respectively). Creatine and guanidinoacetate concentrations tended to be higher in hemodialysis patients and lower in the undialyzed group of patients with chronic renal failure. This procedure provides a rapid, sensitive, and accurate method for the study of guanidine metabolism in persons with uremia.

Arginine↗
PubMed1976

[Participation of the beta-receptor system in the genesis of the carotid aortic baroreceptor reflex in the dog (author's transl)].

The effects of propranolol, given by close arterial injection, on the reflex vasodilatation induced in the atropinized isolated gracilis muscle by rapid i.v. administration of norepinephrine were studied in dogs. The integrated areas of vasodilatation were significantly reduced after treatment with propranolol. Thus the conclusion was that adrenergic beta-receptors participate in the reflex vasodilatation, although how they act needs further elucidation.

Animals↗
PubMed1975

Studies on the nature of the vasodilator fibers running in the lumbar sympathetic chain of the dog.

These experiments were performed to further elucidate the nature of the vasodilator fibers running in the sympathetic chain in the dog. The electrostimulation of the lumbar sympathetic trunk caused vasoconstriction in the perfused hind limb which inverted to vasodilatation after guanethidine was administered. This vasodilator response is mediated by cholinergic fibers since it was completely abolished by atropine. The observation, furthermore, that hexamethonium completely nullified both vasodilator and vasoconstrictor responses to the electrostimulation of the sympathetic chain indicates that both vasoconstrictor and vasodilator fibers, which are activated during the stimulation of the sympathetic chain, are preganglionic in nature.

Animals↗
PubMed1975

Studies on the hemodynamic changes induced by electrical stimulation of the vagosympathetic trunks in the dog.

The effects of electrostimulation of the cephalic endings of the vago-sympathetic trunks on the systemic and perfusion pressure of the hind limb of the dog depend upon frequency, intensity and duration of the stimulus. The electrostimulation performed with stimuli of high frequency, low intensity and moderately long duration (rectangular waves of 1.5 V, 0.7 msec, 100 Hz) consistently elicited systemic hypertension and vasoconstriction. This response was completely abolished by pretreatment with guanethidine or hexamethonium. On the other hand, electrostimulation with stimuli of low frequency, high intensity and long duration (5 V, 1 msec, 10 Hz) produced systemic hypotension and vasodilatation in the perfused hind limb. These effects were completely blocked by atropine or hexamethonium, while guanethidine was unable to induce any modification. These findings suggest that electrostimulation of vagosympathetic trunks can evoke different hemodynamic responses depending upon the characteristics of the stimulus. The occurrence of a vasodilatation specifically blocked by atropine demonstrates that a purely cholinergic mechanism underlies such a reflex response.

Animals↗
PubMed1975

Reduction of circulating insulin levels during the infusion of different prostaglandins in the rat.

The intravenous infusion of prostaglandin (PG) E1, E2, and A1 into normal rats at a dose of 2 mug/min significantly lowered plasma insulin levels with a tendency to recovery in the post infusion period. Whereas PGA1 infusion resulted in a moderate but significant hypoglycaemia, the administration of E-series PGs always produced a hyperglycaemic effect. The interference of PGE1 on insulin response to classical insulinogogues (glucagon, aminophylline, and tolbutamide) was also investigated. The results of these experiments demonstrate that PGE1 exerts an inhibitory action on insulin response to all insulin releasing agents investigated. As regards the haemodynamic effects of PGs, PGE1 and PGE2 lowered the arterial blood pressure by about 20 percent, while PGA1 was almost completely ineffective. On the other hand, the lowering effect of PGE1 on circulating insulin levels remained unchanged in rats treated with reserpine. These findings thus rule out a sympathetic over-activity secondary to the lowered arterial blood pressure as the mechanism of action of PGE1. A possible direct interference with the adrenergic receptor system of the pancreatic islets was also ruled out since the inhibitory effect of PGE1 was not overcome by phentolamine pre-treatment.

Aminophylline↗
PubMed1975

Effects of theophylline on glucose kinetics in normal and sympathectomized rats.

The influence of intraperitoneal administration of aminophylline on the rate of hepatic glucose production and peripheral uptake (Ra and Rd) was studied in normal and in adrenodemedullated and reserpinized rats by using the primed constant infusion of Glucose-2-3H. In normal rats, the dose of 100 mg. per kilogram of aminophylline produced a marked increase of Ra and Rd. Since Ra rose more rapidly than Rd did initially, hyperglycemia developed. Thereafter, glucose production and uptake increased to nearly the same extent, and a new steady state was reached at plasma glucose levels almost twice those of the baseline. Smaller and transient modifications were observed after the administration of 20 mg. per kilogram of aminophylline. With the higher dose, insulin levels markedly rose (reaching a tenfold peak above the basal value) while minor increments were observed with the lower dose. In a group of normal rats which were given glucose (10 mg. per kilogram per minute) in order to achieve a degree of hyperglycemia comparable to that brought about by the higher dose of aminophylline, an almost identical enhancement of glucose uptake was recorded. However, insulin levels were much higher in aminophylline-treated rats as compared to normal rats. From these finding it was concluded that aminophylline induces resistance to insulin effect. When aminophylline was injected into demedullated rats pretreated with reserpine, at the dose of 100 mg. per kilogram, a marked enhancement of Ra, and consequently of glycemia, was recorded initially; later, severe hypoglycemia developed depending on both a progressive exhaustion of hepatic glucose production and a marked increase of glucose utilization. Insulin levels dramatically increased in these experiments. These results suggest that aminophylline directly increases glucose production by the liver and insulin secretion. The simultaneous activation of the sympathetic system blunts the insulin response and counteracts the restraining effect of insulin on the liver and the stimulatory effect of insulin on overall glucose uptake as well.

Adrenal Medulla↗
PubMed1975

The effect of dexamethasone on urinary acidification.

Although it is well recognized that mineralocorticoids enhance renal acid excretion, the effect of glucocorticoids on renal acidification is unclear. Oral administration of dexamethasone to six healthy volunteers for 1 week at a daily dose of 4.5 mg was associated with mild respiratory alkalosis and a small but statistically significant increase in baseline urine pH. However, neither the ability to lower urine pH nor to excrete titratable acid and ammonium after NH4Cl acid-loading was altered. Administration of a single intravenous dose of dexamethasone sodium phosphate (7.5 mg) was associated with a significant rise in urine pH and potassium excretion and decreased titratable acid, ammonium , and phosphorus excretion in the absence of changes in blood acid-base status, creatinine clearance, or urine flow.

Adolescent↗